摘要
目的研究甘草酸对压力超负荷诱导的心肌肥厚的作用及其机制。方法将40只C57BL/6小鼠随机分成假手术+生理盐水组、假手术+甘草酸组、手术+生理盐水组和手术+甘草酸组,每组10只。通过主动脉缩窄术诱导小鼠心肌肥厚,术后分别给以连续4 w生理盐水或甘草酸灌胃治疗。采用超声检测评价小鼠心功能,HE染色和天狼星红染色等组织病理学方法评价心肌肥厚及纤维化程度,Western Blot检测磷酸化丝裂原活化蛋白激酶(MAPK)和MAPK总蛋白。结果主动脉缩窄术4 w后,手术+甘草酸组小鼠的心功能相关指标较手术+生理盐水组明显改善,心肌肥厚和纤维化相关组织病理学指标也明显降低,且细胞外信号调节激酶(ERK1/2)磷酸化水平明显降低。而假手术+生理盐水组与假手术+甘草酸组之间上述各指标均无明显差异。结论甘草酸具有抗压力超负荷诱导的心肌肥厚和纤维化,其机理可能与抑制ERK1/2信号通路有关。
Objective To study whether glycyrrhizin would attenuate cardiac hypertrophy through blocking the mitogen- activated protein kinase （MAPK） signaling. Methods Aortic banding （AB） mice model were used in testing the hypothe- sis. 40 Mice were grouped into four groups （ 10 mice per group） ： Sham （ saline）, Sham ＋ glycyrrhizin, AB （saline） and AB ＋ Glycyrrhizin group. Normal saline intragastric administration was served in the Sham （saline） and AB （saline） groups. After surgery, mice of the Sham ＋ glycyrrhizin and AB ＋ glycyrrhizin groups were given an intragastric administration with gly- cyrrhizin at a dose of 1130 mg . kg-1 . d-1 for up to 4 weeks. Doppler analysis was performed to measure the cardiac fuction. Sections of heart were stained with hematoxylin and eosin for histopathology or picrosirius red for collagen deposition. Western blots were performed to detect the phosphorylative activation of MAPKs. Results Compare to the AB group, the cardiac function and the parameters of cardiac hypertrophy and fibrosis were obviously improved in the AB ＋ glycyrrhizin group. Meanwhile, the phosphorylation of extracellular signal-regulated kinasel/2 （ERK1/2） was markedly reduced. All the results of the above parameters had been demonstrated no significant difference in the Sham （saline） and AB （saline） groups. Conclusions Our data suggest that glycyrrhizin is a promising therapeutic agent for cardiac hypertrophy protection that tar- gets the ERK1/2 pathway.
出处
《中国心脏起搏与心电生理杂志》
2012年第6期535-538,共4页
Chinese Journal of Cardiac Pacing and Electrophysiology
关键词
心血管病学
甘草酸
心肌肥厚
丝裂原活化蛋白激酶
Cardiology
Glycyrrhizin
Cardiac hypertrophy
Mitogen-activated protein kinase
